The frequency, pathway of conduction and rate of propagation of action potentials through the heart, which cause the heart to beat in an efficient manner, are controlled by specialized groups of cardiac cells which form the cardiac conduction system. This special conduction system includes the sinoatrial node (SA node), the atrial internodal tracts, the atrioventricular node (AV node), the His bundle, and the right and left bundle branches.
The SA node, located at the junction of the superior vena cava and right atrium, normally acts as the natural pacemaker, generating action potentials, which are conducted through the rest of the heart. When normal conduction pathways are intact, an action potential generated in the SA node is conducted through the atria and to the AV node via the atrial internodal tracts. The conduction through the AV nodal tissue is takes longer than through the atrial tissue, resulting in a delay between atrial contraction and the start of ventricular contraction.
The AV node, located in the central fibrous body, conducts the action potential to the His bundle, located under the annulus of the tricuspid valve. The His bundle splits into the left and right bundle branches, which are formed of specialized fibers called “Purkinje fibers.” The Purkinje fibers rapidly conduct the action potential down the ventricular septum, spreading the depolarization wavefront quickly through the remaining ventricular myocardium, producing a coordinated contraction of the ventricular muscle mass.
Conduction abnormalities may cause slowed or disrupted conduction anywhere along this conduction pathway. For example, the SA node may not generate action potentials at a fast enough rate resulting in too slow of heart rate, or bradycardia. AV block may prevent conduction of the action potential from the atria to the ventricles. These and other conduction abnormalities may be treated by an external or implantable pacemaker.
Pacemakers are typically coupled to the heart via one or more leads, carrying one or more electrodes for stimulating the heart and for sensing the intrinsic electrical signals associated with a conducted action potential. Electrodes are commonly placed on the endocardial surface using a transvenous approach. For example a right ventricular lead may be advanced into the right ventricle and placed such that an electrode is positioned at or near the right ventricular apex. Low capture thresholds and stable lead positioning have made the right ventricular apex a preferred ventricular stimulation site.
However, ventricular pacing at the location of the right ventricular apex does not mimic the normal ventricular conduction pathway. Both experimental and clinical studies have shown that septal pacing can improve various indices of cardiac function compared to apical pacing. See, for example, Kolettis T M, et al., Chest, 2000; 117:60-64, Rosenquvist M., et al, PACE 1996;19:1279-86, and Takagi Y, et al., PACE 1999; 22:1777-81. Direct myocardial stimulation can cause remodeling of the ventricular myocardium, including myofibrilar disarray and local hypertrophy away from the electrode. See, for example, Karpawich P P et al., PACE. 1999; 22(0):1372-7.
The most normal physiological approach to pacing the ventricles when normal AV nodal conduction fails may be to deliver electrical stimulation pulses directly to the His bundle. Depolarization of the His bundle tissue may be conducted normally through the ventricular conduction pathway, down the left and right bundle branches and to the remainder of the ventricular myocardium. The resulting ventricular contraction, which is more rapid, resulting in a narrow QRS complex and a more vigorous, normal contraction, may produce a better-coordinated contraction for achieving efficient heart pumping action.
The His bundle, however, is surrounded by non-excitable tissue, normally resulting in unacceptably high thresholds for depolarizing, or “capturing” the His bundle tissue. The current field produced around a conventional unipolar or biopolar stimulation electrode may not effectively reach the relatively deep His bundle tissue or penetrate the surrounding non-excitable tissue. Increasing the stimulation energy in an attempt to capture the His bundle can result in capturing other surrounding, excitable tissue. Two leads could be placed adjacent each other near the His bundle so that the tip electrodes could be used as a bipolar pacing pair. However, placement of two leads would require longer surgical time, may not allow for controlled inter-electrode spacing and would increase the number of lead bodies running through a patient's veins. A medical lead is needed, therefore, for delivering stimulation pulses for effectively capturing the His bundle and thereby recruiting the normal ventricular conduction pathway for more physiological contraction dynamics and potentially improved hemodynamics during cardiac pacing.